Oncogenic spiral by infectious pathogens: Cooperation of multiple factors in cancer development

Yasunaga, Jun-ichirou; Matsuoka, Masao

doi:10.1111/cas.13443

Cited by 34 publications

(30 citation statements)

References 79 publications

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“…These subpopulation of cells interact with each other, as well as with neoplastic cells, via complex communication networks through secreted cytokines and chemokines ( 50 ). It has been reported that H. pylori is causally associated with the malignancies of gastric epithelia ( 51 ). H. pylori causes inflammation of the gastric mucosa by inducing gastric epithelial cells to secrete IL-8, resulting in the recruitment of inflammatory cells at the site of infection ( 52 ).…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics and immunohistochemistry analyses of expression levels and clinical significance of CXCL2 and TANs in an oral squamous cell carcinoma tumor microenvironment of Prophyromonas gingivalis infection

et al. 2021

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Section: Discussionmentioning

confidence: 99%

Bioinformatics and immunohistochemistry analyses of expression levels and clinical significance of CXCL2 and TANs in an oral squamous cell carcinoma tumor microenvironment of Prophyromonas gingivalis infection

et al. 2021

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“…Persistent infections are important causes of chronic inflammation leading to malignant diseases; up to 25% of human cancers are thought to be associated with infectious agents (10,11).…”

mentioning

confidence: 99%

HTLV-1 induces T cell malignancy and inflammation by viral antisense factor-mediated modulation of the cytokine signaling

Higuchi

Yasunaga

Mitagami

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of a T cell neoplasm and several inflammatory diseases. A viral gene, HTLV-1 bZIP factor (HBZ), induces pathogenic Foxp3-expressing T cells and triggers systemic inflammation and T cell lymphoma in transgenic mice, indicating its significance in HTLV-1–associated diseases. Here we show that, unexpectedly, a proinflammatory cytokine, IL-6, counteracts HBZ-mediated pathogenesis. Loss of IL-6 accelerates inflammation and lymphomagenesis in HBZ transgenic mice. IL-6 innately inhibits regulatory T cell differentiation, suggesting that IL-6 functions as a suppressor against HBZ-associated complications. HBZ up-regulates expression of the immunosuppressive cytokine IL-10. IL-10 promotes T cell proliferation only in the presence of HBZ. As a mechanism of growth promotion by IL-10, HBZ interacts with STAT1 and STAT3 and modulates the IL-10/JAK/STAT signaling pathway. These findings suggest that HTLV-1 promotes the proliferation of infected T cells by hijacking the machinery of regulatory T cell differentiation. IL-10 induced by HBZ likely suppresses the host immune response and concurrently promotes the proliferation of HTLV-1 infected T cells.

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“…A study by Son et al [ 86 ] demonstrated that genipin (70 μM) can have antiviral effects against Epstein–Barr virus (EBV). As EBV causes several human cancers [ 87 , 88 ], an antiviral effect could have implications in the protection against virus-induced carcinogenesis. A study by Cho et al [ 89 ] also showed an effect of genipin against the Kaposi’s sarcoma-associated herpesvirus (KSHV).…”

Section: Anticancer Effects Of Geniposide and Genipinmentioning

confidence: 99%

Plant-Derived Anticancer Agents: Lessons from the Pharmacology of Geniposide and Its Aglycone, Genipin

Habtemariam

Lentini

2018

Biomedicines

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For centuries, plants have been exploited by mankind as sources of numerous cancer chemotherapeutic agents. Good examples of anticancer compounds of clinical significance today include the taxanes (e.g., taxol), vincristine, vinblastine, and the podophyllotoxin analogues that all trace their origin to higher plants. While all these drugs, along with the various other available therapeutic options, brought some relief in cancer management, a real breakthrough or cure has not yet been achieved. This critical review is a reflection on the lessons learnt from decades of research on the iridoid glycoside geniposide and its aglycone, genipin, which are currently used as gold standard reference compounds in cancer studies. Their effects on tumour development (carcinogenesis), cancer cell survival, and death, with particular emphasis on their mechanisms of actions, are discussed. Particular attention is also given to mechanisms related to the dual pro-oxidant and antioxidant effects of these compounds, the mitochondrial mechanism of cancer cell killing through reactive oxygen species (ROS), including that generated through the uncoupling protein-2 (UCP-2), the inflammatory mechanism, and cell cycle regulation. The implications of various studies for the evaluation of glycosidic and aglycone forms of natural products in vitro and in vivo through pharmacokinetic scrutiny are also addressed.

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Oncogenic spiral by infectious pathogens: Cooperation of multiple factors in cancer development

Cited by 34 publications

References 79 publications

Bioinformatics and immunohistochemistry analyses of expression levels and clinical significance of CXCL2 and TANs in an oral squamous cell carcinoma tumor microenvironment of Prophyromonas gingivalis infection

Bioinformatics and immunohistochemistry analyses of expression levels and clinical significance of CXCL2 and TANs in an oral squamous cell carcinoma tumor microenvironment of Prophyromonas gingivalis infection

HTLV-1 induces T cell malignancy and inflammation by viral antisense factor-mediated modulation of the cytokine signaling

Plant-Derived Anticancer Agents: Lessons from the Pharmacology of Geniposide and Its Aglycone, Genipin

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